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Normoxic hypercapnia may increase high-frequency (HF) power in heart rate variability (HRV) and also increase respiratory sinus arrhythmia (RSA). Low-frequency (LF) power may remain unchanged. In this study, 5-min ECG recordings (N = 10) were analyzed in time and frequency domains while human subjects breathed normoxic 5% CO2 (5%CO2) or room air (RA). Tidal volume (VT), inhalatory (TI), and exhalatory (TE) times of breaths in the final minute were measured. ECG time domain measures were unaffected by CO2 inhalation (P &gt; 0.05). Following natural logarithmic transformation (LN), LFLN was unaltered (RA: 7.14 +/- 0.95 vs. 5%CO2: 7.35 +/- 1.12, P &gt; 0.05), and HFLN increased (RA: 7.65 +/- 1.37 vs. 5%CO2: 8.58 +/- 1.11, P &lt; 0.05) with CO2 inhalation. When changes in total power (NU) were corrected, LF(NU) decreased (RA: 34.4 +/- 22.9 vs. 5%CO2: 23.8 +/- 23.1, P &lt; 0.01), and HFNU increased (RA: 56.5 +/- 22.3 vs. 5%CO2: 66.8 +/- 22.9, P &lt; 0.01) with CO2 inhalation. TI (RA: 2.0 +/- 1.0 vs. 5%CO2: 1.9 +/- 0.8 s) and TE (RA: 2.5 +/- 1.1 vs. 5%CO2: 2.4 +/- 0.9 s) remained unchanged, but VT increased with CO2 inhalation (RA: 1.1 +/- 0.3 vs. 5%CO2: 2.0 +/- 0.8 L, P &lt; 0.001). Heart rates during inhalation (RA: 35.2 +/- 4.4, 5%CO2: 34.5 +/- 4.8 beats min(-1)) were different from heart rates during exhalation (RA: 28.8 +/- 4.4, 5%CO2: 29.1 +/- 3.1 beats min(-1)). Hypercapnia did not increase the clustering of heart beats during inhalation, and we suggest that the HF component may not adequately reflect RSA.

Cardiac Vagal Control and Respiratory Sinus Arrhythmia during Hypercapnia in Humans